ristocetin and Anemia--Iron-Deficiency

Platelet aggregation was measured by an optical method in 32 patients with iron-deficiency anemia at the time of diagnosis and after a period of supplementation with iron. Epinephrine- and adenosine diphosphate-induced platelet aggregation were lower in anemic patients than in the controls (p<0.05). After iron-supplementation therapy, these values showed no significant differences. If induced by collagen or ristocetin, platelet aggregation was the same for patients and controls, but increased after treatment of patients (p<0.05). The plasma zinc values did not show significant differences among the subjects included in this study. These results show that iron is involved in the enzymatic systems that regulate platelet aggregation. The exact nature of this interaction is still to be determined.

Topics: Anemia, Iron-Deficiency; Collagen; Dietary Supplements; Female; Humans; Iron; Male; Platelet Aggregation; Ristocetin; Zinc

Iron deficiency anemia (IDA) may cause platelet aggregation dysfunction and this can be reversed by iron therapy. On the other hand, it has been reported that the platelet fractions carrying the platelet activation markers, CD62P and CD63, are increased in thalassemic patients and there is a significant correlation between the increased levels of soluble P-selectin and free iron in sickle cell disease. This study was performed to investigate the alterations of platelet functions and whether iron deficiency results in diminished expression of activation marker (P-selectin; CD62P) leading to platelet aggregation dysfunction in children with IDA. Hemoglobin, erythrocyte indices (mean erythrocyte volume and red blood cell distribution width), serum levels of iron, transferrin and ferritin, platelet aggregation tests (with ADP, collagen, and ristocetin), PFA-100 closure time, and CD62P expression were evaluated in fasting blood samples of 22 children with IDA and 20 children without anemia. CD62P expression was detected by flow cytometry in normal and 5 μmol/l ADP-activated platelets. Mean closure times were longer in the patient group than control. In platelet aggregation tests, mean values of maximum aggregation times by ristocetin, ADP, and collagen were also more prolonged in patient group. Ristocetin-induced maximum aggregation rates (amplitude) were significantly higher in patients. However, ADP and collagen induction did not produce the same effect. CD62P expressions were significantly higher on activated platelets of the patient group, although they were similar in both groups before activation by ADP. These findings suggest that platelet aggregation and adhesion have been delayed in children with IDA; however, platelet function abnormalities are not associated with CD62P expression on platelet surface.

Topics: Adenosine Diphosphate; Anemia, Iron-Deficiency; Blood Platelets; Case-Control Studies; Child; Child, Preschool; Collagen; Erythrocyte Indices; Female; Ferritins; Flow Cytometry; Gene Expression; Hemoglobins; Hemostasis; Humans; Iron; Male; P-Selectin; Platelet Activation; Platelet Aggregation; Platelet Count; Ristocetin; Transferrin

This study was performed to evaluate the effect of iron therapy on platelet function among women with unexplained menorrhagia in order to better understand possible interactions between iron deficiency anemia and platelet behavior and menorrhagia. Platelet aggregation and adenosine triphosphate (ATP) release induced by 5.0 mM adenosine diphosphate (ADP), 0.5 mM arachidonic acid (AA), 1.0 mg/ml ristocetin and 2 microg/ml collagen were studied by whole-blood platelet lumi-aggregometer in 50 menorrhagic women before and after oral iron therapy and in 22 women of the control group. There was a significant increase in AA- induced platelet aggregation (p < 0.05) and a decrease in ristocetin-induced platelet aggregation (p < 0.01) after treatment. Pre- and posttreatment platelet aggregation responses to ADP and collagen were not significantly different (p > 0.05). Pre- and posttreatment platelet secretion responses to all agonists disclosed no significant difference (p > 0.05). There was no significant difference between the study group after treatment and the control group in respect to platelet aggregation and ATP secretion values induced by all agonists (p > 0.05). We conclude that iron deficiency anemia in women causes AA-induced platelet dysfunction, which may give rise to increased menstrual blood loss and can be reversed by iron repletion.

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Anemia, Iron-Deficiency; Arachidonic Acid; Collagen; Female; Humans; Iron; Menorrhagia; Platelet Aggregation; Platelet Function Tests; Ristocetin

Although it is known that platelet count is altered in iron deficiency anaemia (IDA), the qualitative extent of this interference is not well documented. In the present study we investigated platelet aggregation (PA) by impedance and optic methods in IDA. Forty-seven patients (plasma group: 16 boys, 9 girls and whole blood group: 11 boys, 11 girls) with IDA and thirty-one healthy children (plasma group: 6 boys, 10 girls and whole blood group: 6 boys, 9 girls) were enrolled into the study. Template bleeding times were measured by the Ivy method in all children. In the control group whole blood count, serum iron levels, bleeding time and PA were determined. After basal PA was determined in the patients and controls, ferrous sulphate was orally administered to the patients at a dose of 6 mg/kg/24 h for three months. Then, PA tests were performed again in the IDA (test group) patients. Ristocetin-induced PA was suppressed in both plasma and whole blood groups. Inhibition by both collagen (p < 0.05) and ristocetin (p < 0.001)-induced PA was determined by the optic method. Similarly in PA measured by the impedance method a suppression to adenosine diphosphate (p < 0.001) and to ristocetin (p < 0.01) was found. However, no significant alteration was observed in the bleeding time. All defective responses were reversed by the iron supplementation therapy. In addition, a significant correlation was found between some parameters of PA and several haematological values. In conclusion, although defective PA responses cannot be clinically demonstrated in patients with IDA, this suppression of PA may be detected by laboratory examination. Therefore, it is advised that care should be taken when using anti-aggregant agents in IDA.

Topics: Adenosine Diphosphate; Anemia, Iron-Deficiency; Blood Cell Count; Blood Coagulation Tests; Child; Child, Preschool; Collagen; Electric Impedance; Epinephrine; Erythrocyte Indices; Female; Ferritins; Hemoglobins; Humans; Infant; Male; Platelet Aggregation; Platelet Function Tests; Ristocetin; Spectrum Analysis; Transferrin